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Mass spectrometry of clinically-discarded preimplantation embryos

ABSTRACT: Clinically-discarded oocytes and preimplantation embryos at various stages were collected to perform proteome analysis.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Embryo

SUBMITTER: ying yin

LAB HEAD: Li-quan Zhou

PROVIDER: PXD042633 | Pride | 2025-05-26

REPOSITORIES: Pride

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			Action	DRS
	21P14040001.raw	Raw
	21P14040002.raw	Raw
	21P14040003.raw	Raw
	21P14040004.raw	Raw
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Publications

Mitofusin 1 Drives Preimplantation Development by Enhancing Chromatin Incorporation of Histone H3.3.

Shi Xiao-Yan XY Tian Yu Y Wang Yu-Fan YF Zhang Yi-Ran YR Yin Ying Y Tian Qing Q Li Lei L Ma Bing-Xin BX He Ximiao X Zhou Li-Quan LQ

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20250316 18

Mitofusin 1 (MFN1) plays a crucial role in mitochondrial fusion and oocyte development. However, its function in preimplantation embryonic development and its potential involvement in epigenetic regulation remain poorly understood. In this study, it is shown that MFN1 interacts with PADI6, a key component of the cytoplasmic lattice in oocytes and early embryos. MFN1 deficiency in mice results in reduced PADI6 levels and decreased expression of translational machinery components, which suppress p ...[more]

PMID: 40091361

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Beclin 1 prevents ISG15-mediated cytokine storms to secure fetal hematopoiesis and survival

Project description:Proper control of inflammatory responses is essential for embryonic development, but the underlying mechanism is poorly understood. Here, we show that under physiological conditions, inactivation of ISG15, an inflammation amplifier, is associated with the interaction of Beclin 1 (Becn1), via its ECD domain, with STAT3 in the major fetal hematopoietic organ of mice. Conditional loss of Becn1 caused sequential dysfunction and exhaustion of fetal liver hematopoietic stem cells, leading to lethal inflammatory cell-biased hematopoiesis in the fetus. Molecularly, the absence of Becn1 resulted in the release of STAT3 from Becn1 tethering and subsequent phosphorylation and translocation to the nucleus, which in turn directly activated the transcription of ISG15 in fetal liver hematopoietic cells, coupled with increased ISGylation and production of inflammatory cytokines, whereas inactivating STAT3 reduced ISG15 transcription and inflammation but improved hematopoiesis potential, and further silencing ISG15 mitigated the above collapse in the Becn1 null hematopoietic lineage. The Becn1-STAT3-ISG15 axis remains functional in Atg5/7-disrupted fetal hematopoietic organs. These results suggest that Becn1, in an autophagy-independent manner, secures hematopoiesis and survival of the fetus by directly inhibiting STAT3-ISG15 activation to prevent cytokine storms. Our findings highlight a previously undocumented role of Becn1 in governing ISG15 to safeguard the fetus.

2025-05-07 | PXD057003 | Pride

Comparative proteomic landscapes provide insights into mammalian preimplantation development and failure

Project description:Understanding mammalian preimplantation development, particularly in humans, at the proteomic level remains limited. Here, we applied our comprehensive solution of ultrasensitive proteomic technology to measure the proteomic profiles of oocytes and early embryos and identified nearly 8,000 proteins in humans and over 6,300 proteins in mice. We observed distinct proteomic dynamics before and around zygotic genome activation (ZGA) between the two species. Integrative analysis with translatomic data revealed extensive divergence between translation activation and protein accumulation. Multi-omic analysis indicated that ZGA transcripts often contribute to protein accumulation in blastocysts. Using mouse embryos, we identified several transcriptional regulators critical for early development, thereby linking ZGA to the first lineage specification. Furthermore, single-embryo proteomics of poor-quality embryos from over 100 patient couples provided insights into preimplantation development failure. Our study may contribute to reshaping the framework of mammalian preimplantation development and opening avenues for addressing human infertility.

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Preimplantation Factor Effect on Endometrial and Decidual Cells

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Paternal under and over nutrition modify semen composition and preimplantation embryo developmental kinetics in mice

Project description:Poor parental health can influence the development and eventual health outcomes of their offspring. Many studies have detailed the maternal role yet a father’s health requires further examination as his poor nutritional status has also been shown to have negative consequences on fetal development and impact the long-term health of his offspring. The present study examined how preimplantation embryo development was altered by sub-optimal paternal diet, with specific focus on sperm- and seminal plasma-mediated mechanisms. To address this, male mice were fed a diet to model either under (low protein diet (LPD)) or over (high fat/sugar ‘Western’ diet (WD)) nutrition, LPD or WD supplemented with methyl-donors or a control diet (CD) before mating. Embryo development was assessed using in vitro time-lapse imaging of preimplantation embryos which revealed a significant increase in embryo development rates in all experimental groups when compared to CD embryos. Further analysis of the semen revealed a significant number of differentially expressed seminal plasma proteins in all groups (LPD: 13, MD-LPD: 27, WD: 24, MD-WD: 19) when compared to control. This study highlights a role for paternal nutritional status influencing embryonic development and the maternal reproductive tract via changes to his metabolic and reproductive health. These findings demonstrate potential direct (sperm-mediated) and indirect (seminal plasma-mediated) pathways in which a father's poor diet could shape the long-term health of his offspring

2024-07-25 | PXD044980 | Pride